ArticleInfection and immunity2007
Resistance to Pseudomonas aeruginosa chronic lung infection requires cystic fibrosis transmembrane conductance regulator-modulated interleukin-1 (IL-1) release and signaling through the IL-1 receptor.
Article in Infection and immunity, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
42 citing papers in PubMed, 68 citations in OpenAlex.
- Targeting inflammasome, IL-1β, and coagulation in melioidosis.Frontiers in microbiology · 2026Review
- Effects of CFTR-ENaC on spinal cord edema after spinal cord injury.Open medicine (Warsaw, Poland) · 2024Article
- Article
- NLRP3 inflammasome activation in cigarette smoke priming for Pseudomonas aeruginosa-induced acute lung injury.Redox biology · 2022Article
- Pseudomonas Aeruginosa Lung Infection Subverts Lymphocytic Responses through IL-23 and IL-22 Post-Transcriptional Regulation.International journal of molecular sciences · 2022Article
- Article
- Integrated evaluation of lung disease in single animals.PloS one · 2021Article
- The Pseudomonas aeruginosa protease LasB directly activates IL-1β.EBioMedicine · 2020Article
- Opposing Effects of IL-1Ra and IL-36Ra on Innate Immune Response toJournal of immunology (Baltimore, Md. : 1950) · 2018Article
- Cystic fibrosis swine fail to secrete airway surface liquid in response to inhalation of pathogens.Nature communications · 2017Article
- Cytokine-Regulation of NaFrontiers in immunology · 2017Review
- Bacterial Secretant fromFrontiers in immunology · 2017Article
- IL-1 receptor antagonist ameliorates inflammasome-dependent inflammation in murine and human cystic fibrosis.Nature communications · 2016Article
- CFTR Controls the Activity of NF-κB by Enhancing the Degradation of TRADD.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2016Article
- Pseudomonas aeruginosa triggers CFTR-mediated airway surface liquid secretion in swine trachea.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- siRNA-mediated gene silencing of MexB from the MexA-MexB-OprM efflux pump in Pseudomonas aeruginosa.BMB reports · 2014Article
- Role of Interleukin-17 in defense against pseudomonas aeruginosa infection in lungs.International journal of clinical and experimental medicine · 2014Article
- Article
- Structure and function of the Type III secretion system of Pseudomonas aeruginosa.Current protein & peptide science · 2012Review
- Role of MexA-MexB-OprM efflux pump system in chronic Pseudomonas aeruginosa pulmonary infection in mice.Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban · 2012Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Innate immunity is critical for clearing Pseudomonas aeruginosa from the lungs. In response to P. aeruginosa infection, a central transcriptional regulator of innate immunity-NF-kappaB-is translocated within 15 min to the nuclei of respiratory epithelial cells expressing wild-type (WT) cystic fibrosis (CF) transmembrane conductance regulator (CFTR). P. aeruginosa clearance from lungs is impaired in CF, and rapid NF-kappaB nuclear translocation is defective in cells with mutant or missing CFTR. We used WT and mutant P. aeruginosa and strains of transgenic mice lacking molecules involved in innate immunity to identify additional mediators required for P. aeruginosa-induced rapid NF-kappaB nuclear translocation in lung epithelia. We found neither Toll-like receptor 2 (TLR2) nor TLR4 nor TLR5 were required for this response. However, both MyD88-deficient mice and interleukin-1 receptor (IL-1R)-deficient mice failed to rapidly translocate NF-kappaB to the nuclei of respiratory epithelial cells in response to P. aeruginosa. Cultured human bronchial epithelial cells rapidly released IL-1beta in response to P. aeruginosa; this process was maximized by expression of WT-CFTR and dramatically muted in cells with DeltaF508-CFTR. The IL-1R antagonist blocked P. aeruginosa-induced NF-kappaB nuclear translocation. Oral inoculation via drinking water of IL-1R knockout mice resulted in higher rates of lung colonization and elevated P. aeruginosa-specific antibody titers in a manner analogous to that of CFTR-deficient mice. Overall, rapid IL-1 release and signaling through IL-1R represent key steps in the innate immune response to P. aeruginosa infection, and this process is deficient in cells lacking functional CFTR.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.